Journal
JOURNAL OF COMPARATIVE NEUROLOGY
Volume 516, Issue 4, Pages 291-311Publisher
WILEY
DOI: 10.1002/cne.22111
Keywords
potassium channels; striate cortex; GABAergic; dual-labeling; immunofluorescence; calcium-binding proteins; parvalbumin; Meynert cells; spiny neurons; excitatory neurons
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Funding
- National Institutes of Health (NIH) [EY-08300, EY-015549, EY-017945, EY P031-13079, NS30989, NS045217]
- NSF [IBN-0314645]
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Voltage-gated potassium channels that are composed of Kv3 subunits exhibit distinct electrophysiological properties: activation at more depolarized potentials than other voltage-gated K+ channels and fast kinetics. These channels have been shown to contribute to the high-frequency firing of fast-spiking (FS) GABAergic interneurons in the rat and mouse brain. In the rodent neocortex there are distinct patterns of expression for the Kv3.1b and Kv3.2 channel subunits and of coexpression of these subunits with neurochemical markers, such as the calcium-binding proteins parvalbumin (PV) and calbindin D-28K (CB). The distribution of Kv3 channels and interrelationship with calcium-binding protein expression has not been investigated in primate cortex. We used immunoperoxidase and immunofluorescent labeling and stereological counting techniques to characterize the laminar and cell-type distributions of Kv3-immunoreactive (ir) neurons in macaque V1. We found that across the cortical layers approximate to 25% of both Kv3.1b- and Kv3.2-ir neurons are non-GABAergic. In contrast, all Kv3-ir neurons in rodent cortex are GABAergic (Chow et al. [1999] J Neurosci. 19:9332-9345). The putatively excitatory Kv3-ir neurons were mostly located in layers 2, 3, and 4b. Further, the proportion of Kv3-ir neurons that express PV or CB also differs between macaque V1 and rodent cortex. These data indicate that, within the population of cortical neurons, a broader population of neurons, encompassing cells of a wider range of morphological classes may be capable of sustaining high-frequency firing in macaque V1. J. Comp. Neurol. 516:291-311, 2009. (C) 2009 Wiley-Liss, Inc.
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